Cardio part 3 Flashcards
(38 cards)
Pathophys of peripheral vascular dz
Primarily the result of atherosclerosis
May manifest acutely when thrombi, emboli, or acute trauma compromises perfusion
Etiology of PVD
Coexisting conditions: CAD AFib Cerebrovascular dz Renal disease RFs: Smoking HLD DM Hyperviscosity
Hx-PVD
Intermittent claudication may be the sole manifestation of early symptomatic PVD
Aortoiliac- pain in the thigh and buttock
Femoropopliteal- pain in the calf
Could also present as the hip or leg “giving out” after a certain period of exertion
Pain does not usually occur with sitting or standing
Ischemic rest pain is more worrisome
Erectile dysfunction can be a potential early indicator
Leriche syndrome- intermittent claudication, impotence, and significantly decreased or absent femoral pulses
PE of PVD
Pulselessness Paralysis Paresthesia Pain Pallor Check all pulses Do Allen test Skin may have an atrophic, shiny appearance and may demonstrate trophic changes
Workup of PVD
CBC CMP Doppler CT may be of use to emergency med if MRI cannot be used ABI
Tx of PVD
Attention to the ABCs, IV access, and obtaining baseline lab studies
Obtain EKG and CXR
Tx of thrombi or emboli- heparin
Consider surgical referral with acute leg pain correlated with a cool distal extremity, diminished or absent distal pulses, and an ankle blood pressure <50 mm Hg
Pathophys of aortic stenosis
When the valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta
Etiology of aortic stenosis requiring surgery
Common causes <70 yo in order: Bicuspid AV Postinflammatory Degenerative Unicommisural Hypoplastic Indeterminate Common causes >70 yo in order: Degenerative Bicuspid Postinflammatory Hypoplastic
H/o aortic stenosis
Usually has an asymptomatic latent period of 10-20 years MC initial complaint is dyspnea CP Heart failure Syncope
PE of aortic stenosis
Carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude and gradual downslope (pulsus parvus et tardus)
Jugular venous pulse may show prominent a waves
A2 usually diminished or absent
Paradoxical splitting of the S2
Prominent S4 can be present
Crescendo-decrescendo systolic murmur
Rough low-pitched sound that is best heard at the second intercostal space in right upper sternal border
Radiates to carotid artery
Workup of aortic stenosis
EKG CXR CMP Cardiac markers CBC TTE Cardiac cath and coronary arteriography BNP
Tx of aortic stenosis
Address ABCs
Perform CPR if in cardiac arrest
With acute sx, hospital admission, telemetry/ICU admission, and cardiology consultation should be considered
Heart failure- oxygen, cardiac and oximetry monitoring, IV access, loop diuretics, nitrates, morphine, and ventilatory support
Percutaneous balloon valvuloplasty is used as a palliative measure
Aortic valve replacement
Pathophys of aortic regurgitation- acute
The LV does not have sufficient time to dilate in response to the sudden increase in volume. As a result, LV end-diastolic pressure increases rapidly, causing an increase in pulmonary venous pressure and altering coronary flow dynamics. As pressure increases throughout the pulmonary circuit, the pt develops dyspnea and pulmonary edema.
Pathophys of aortic regurgitation- chronic
Chronic AR causes gradual left ventricular volume overload that leads to a series of compensatory changes, including LV enlargement and eccentric hypertrophy. LV dilation occurs through the addition of sarcomeres in series, as well as through the rearrangement of myocardial fibers. As a result, the LV becomes larger and more compliant, with greater capacity to deliver a large stroke volume that can compensate for the regurgitant volume
Etiology of acute aortic regurgitation
Infective endocarditis Chest trauma Post-TAVR LVAD implantation Aortic dissection Prosthetic valve malfunction
Etiology of chronic aortic regurgitation
Bicuspid aortic valve Certain wt loss meds, such as fenfluramine and dexfenfluramine Rheumatic fever Ankylosing spondylitis Behcet dz Giant cell arteritis RA SLE Takayasu arteritis Whipple disease Marfan syndrome Ehlers-Danlos syndrome Floppy aortic valve Aortic valve prolapse Sinus of Valsalva aneurysm Aortic annular fistula
H/o acute aortic regurgitation
Sudden, severe SOB
Rapidly developing HF
CP
H/o chronic aortic regurgitation
Long-standing asymptomatic period that may last for several years Compensatory tachycardia may develop Severe chronic AR: -Palpitations -Uncomfortable awareness of the heartbeat -SOB -CP -Sudden cardiac death
PE of acute aortic regurgitation
Tachycardia Peripheral vasoconstriction Cyanosis Pulmonary edema Arterial pulses alternans Early decrescendo diastolic murmur best heard leaning forward in full expiration Austin-Flint murmur
PE of chronic aortic regurgitation
DBP <60, with pulse pressures often exceeding 100 mm Hg
Becker sign
Corrigan pulse
de Musset sign
Hill sign
Duroziez sign
Muller sign
Quincke sign
Traube sign
PMI may be diffuse or hyperdynamic but is often displaced inferiorly and toward the axilla
Peripheral pulses are prominent or bounding
S3 gallop if LV dysfunction is present
High-pitched murmur that is loudest at the left sternal border
Austin-Flint murmur
Becker sign
Visible systolic pulsations of the retinal arterioles
Corrigan pulse
Abrupt distention and quick collapse on palpation of the peripheral arterial pulse
de Musset sign
Bobbing motion of the pt’s head with each heartbeat
Hill sign
Popliteal cuff systolic BP 40 mm Hg higher than brachial cuff SBP
